Department of Endocrinology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road 246, Harbin 150086, Heilongjiang, China.
Department of Endocrinology, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road 246, Harbin 150086, Heilongjiang, China.
Hum Immunol. 2021 Dec;82(12):960-967. doi: 10.1016/j.humimm.2021.08.010. Epub 2021 Sep 15.
To explore the effect of LINC00323 on the polarization of M1 macrophages in diabetic nephropathy. To study the effect and biological mechanism of LINC00323 on the occurrence and development of diabetic nephropathy.
We used clinical samples to analyze the correlation between macrophage polarization and the occurrence and development of diabetic nephropathy. In addition, we used bioinformatics to analyze the key molecules of macrophage polarization. We then verified the key pathways that promote the M1 polarization of macrophages at the level of cell biology. And we verify the effectiveness of treatment against this target in animal experiments.
We analyzed in clinical samples that the expression of inflammatory factors (TNF-α and IL-6) increased in patients with diabetic nephropathy. In addition, we found that the expression of M1 marker protein CD86 increased through PCR and western blot analysis. We found a key target (LINC00323) through bioinformatics. The expression of LINC00323 in patients' blood samples is also at a high level. We further explored the mechanism of LINC00323 involved in the polarization of M1 macrophages at the level of cellular molecular biology, and found that it is closely related to the PI3K/AKT signaling pathway. In animal models, we found that inhibiting the expression of LINC00323 can reduce the damage of diabetic nephropathy.
We found that LINC00323 mediates the polarization of M1 macrophages through the PI3K/AKT signaling pathway. LINC00323 plays an important role in the occurrence and development of diabetic nephropathy.
探讨 LINC00323 对糖尿病肾病中 M1 巨噬细胞极化的影响。研究 LINC00323 对糖尿病肾病发生发展的影响及其生物学机制。
我们使用临床样本分析巨噬细胞极化与糖尿病肾病发生发展的相关性。此外，我们使用生物信息学分析巨噬细胞极化的关键分子。然后，我们在细胞生物学水平上验证促进巨噬细胞 M1 极化的关键途径，并在动物实验中验证针对该靶点的治疗效果。
我们在临床样本中分析发现，糖尿病肾病患者的炎症因子（TNF-α 和 IL-6）表达增加。此外，我们通过 PCR 和 western blot 分析发现 M1 标志物蛋白 CD86 的表达增加。我们通过生物信息学发现了一个关键靶点（LINC00323）。患者血液样本中 LINC00323 的表达也处于高水平。我们进一步在细胞分子生物学水平上探讨了 LINC00323 参与 M1 巨噬细胞极化的机制，发现它与 PI3K/AKT 信号通路密切相关。在动物模型中，我们发现抑制 LINC00323 的表达可以减轻糖尿病肾病的损伤。
我们发现 LINC00323 通过 PI3K/AKT 信号通路介导 M1 巨噬细胞的极化。LINC00323 在糖尿病肾病的发生发展中起重要作用。
